Search

Soybean oil (SO)-, SO medium-chain triglyceride (MCT)-, olive oil (OO)-, and fish oil (FO)-based lipid emulsions are generally applied in clinical practice via intravenous injection for patients with nutritional requirements. The function of lipid emulsions on immune modulation remains inconsistent, and their effects on macrophages are limited. In the present study, we used a model of S. aureus-infected mouse RAW264.7 macrophages to determine the influence of three different compositions of lipid emulsions (Lipofundin, ClinOleic, and Omegaven) on reactive oxygen species (ROS) production, phagocytosis, and bacterial survival. The three individual lipid emulsions similarly enhanced bacterial survival but reduced S. aureus-stimulated ROS, phagocytosis of S. aureus bioparticles conjugate, polymerization of F-actin, and phosphorylation of AKT, JNK, and ERK. Compared with the JNK and ERK inhibitors, the PI3K inhibitor markedly suppressed the phagocytosis of S. aureus bioparticles conjugate and the polymerization of F-actin, whereas it significantly increased the bacterial survival. These results suggest that the three lipid emulsions diminished ROS production and phagocytosis, resulting in increased bacterial survival. PI3K predominantly mediated the inhibitory effects of the lipid emulsions on the phagocytosis of mouse RAW264.7 macrophages.

Soybean oil (SO)-, SO medium-chain triglyceride (MCT)-, olive oil (OO)-, and fish oil (FO)-based lipid emulsions are generally applied in clinical practice via intravenous injection for patients with nutritional requirements. The function of lipid emulsions on immune modulation remains inconsistent, and their effects on macrophages are limited. In the present study, we used a model of S. aureus-infected mouse RAW264.7 macrophages to determine the influence of three different compositions of lipid emulsions (Lipofundin, ClinOleic, and Omegaven) on reactive oxygen species (ROS) production, phagocytosis, and bacterial survival. The three individual lipid emulsions similarly enhanced bacterial survival but reduced S. aureus-stimulated ROS, phagocytosis of S. aureus bioparticles conjugate, polymerization of F-actin, and phosphorylation of AKT, JNK, and ERK. Compared with the JNK and ERK inhibitors, the PI3K inhibitor markedly suppressed the phagocytosis of S. aureus bioparticles conjugate and the polymerization of F-actin, whereas it significantly increased the bacterial survival. These results suggest that the three lipid emulsions diminished ROS production and phagocytosis, resulting in increased bacterial survival. PI3K predominantly mediated the inhibitory effects of the lipid emulsions on the phagocytosis of mouse RAW264.7 macrophages. [ABSTRACT FROM AUTHOR]